The effects of alcohol on coagulation and fibrinolytic factors: a controlled trial
The effects of alcohol on coagulation and fibrinolytic factors: a controlled trial
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DOI：
10.1097/00001721-199801000-00005
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发表时间：
1998-01-01
影响因子：
1.1
通讯作者：
Beilin, LJ
中科院分区：
文献类型：
--
作者：
Dimmitt, SB;Rakic, V;Beilin, LJ
轻度至中度酒精摄入与缺血性心血管事件发生率降低相关，而重度酒精摄入可使个体易患中风。酒精引起的凝血和纤维蛋白溶解的变化可能是相关的，并且是55名主要饮用啤酒的男性中不同酒精摄入量的对照试验的主题。在保持正常饮酒习惯4周稳定后，参与者被随机分配继续正常饮酒或通过改为低酒精啤酒限制饮酒4周。在最后的4周内，他们分别转换为低酒精摄入或正常酒精摄入。比较低酒精和通常酒精的组合时期，平均每周酒精摄入量从92毫升增加到410毫升，（平均每日摄入量为13至58 ml）与血浆纤维蛋白原降低相关（11%，P < 0.001）和血小板计数（3%，P < 0.05），但因子VII增加（7%，P = 0.001）、组织型纤溶酶原激活物（tPA; 16%，P = 0.01）和纤溶酶原激活物抑制物-1（派-1; 21%，P < 0.001）。tPA/派-1比值从0.50降至0.44（P = 0.02），证实了派-1随着饮酒的增加而相对较大。两种脂质相关的天然抗凝剂，组织因子途径抑制剂和β（2）-糖蛋白-I，没有变化。酒精摄入后血浆纤维蛋白原的显著降低可能有助于酒精对缺血性冠状动脉和脑事件的明显保护作用。与tPA相比，酒精摄入增加因子VII和派-1相对较大的增加可能会削弱这种益处，并且确实可能使个体易于血栓形成，从而导致重度饮酒者中缺血性卒中的发生率增加。任何个体的抗凝血、促凝血和纤溶作用的平衡可能会因摄入酒精饮料的数量和类型以及遗传和其他变量而异，所有这些都值得进一步研究。(C)1998 Rapid Science Ltd.
Light-to-moderate alcohol intake is associated with a reduced incidence of ischaemic cardiovascular events, whilst heavy alcohol intake can predispose individuals to stroke. Alcohol-induced changes in coagulation and fibrinolysis may be relevant and are the subject of this controlled trial of varying alcohol intake in 55 predominantly beer-drinking men. Following 4 weeks stabilization maintaining usual drinking habits, participants were randomized to either continue usual alcohol intake or to restrict alcohol by changing to low alcohol beer for 4 weeks. In a final 4 week period, they crossed over to low or usual alcohol intake, respectively. Comparing combined low and usual alcohol periods, an increase in mean weekly alcohol intake from 92 to 410 ml (mean daily intake from 13 to 58 ml) was associated with a decrease in plasma fibrinogen (by 11%, P < 0.001) and platelet count (3%, P < 0.05), but increases in factor VII (7%, P = 0.001), tissue plasminogen activator (tPA; 16%, P = 0.01) and plasminogen activator inhibitor-1 (PAI-1; 21%, P < 0.001). The ratio, tPA/PAI-1, fell from 0.50 to 0.44 (P = 0.02) confirming the relatively greater increase in PAI-1 , with alcohol consumption. Two lipid-associated natural anticoagulants, tissue factor pathway inhibitor and beta(2)-glycoprotein-I, did not change. The substantial reduction in plasma fibrinogen with alcohol intake may well contribute to the apparent protection alcohol confers against ischaemic coronary and cerebral events. The increase in factor VII and relatively greater increase in PAI-1 than tPA with alcohol intake may attenuate this benefit and indeed may sufficiently predispose individuals to thrombosis to contribute to the increased incidence of ischaemic stroke seen in heavier drinkers. The balance of anticoagulant and procoagulant and fibrinolytic effects in any individual may vary depending on quantity and type of alcoholic beverage ingested, as well as on genetic and other variables, all of which merit further study. (C) 1998 Rapid Science Ltd.